Given that p73 is lost or silenced in human B-cell lymphomas, the Mdm2(Tg);p73(+/-) mouse serves as a model for human disease and may provide additional insight into the pathways that contribute to B-cell lymphomagenesis.
In the current review, we will provide an overview of recent progress discussing the role of TP73 in cancer, specifically addressing its relevance to lymphomagenesis, progression, therapy resistance, and its potential as a novel therapeutic target.
Thus, it is presumed that mutation of p73 might lead to production of defective p73 protein and this might have a role in the process of leukemogenesis of ALL.
Thus, it is presumed that mutation of p73 might lead to production of defective p73 protein and p73 mRNA, and this might have a role in the process of leukemogenesis of AML.
Rearrangements involving the 1p36 chromosomal region occur frequently in NHL, suggesting the existence of tumor suppressor gene(s) that are important in lymphomagenesis. p73 is closely related to the tumor suppressor p53 and maps to the chromosome 1p36 region.